In acute myeloid leukemia (AML), the microenvironmental control on the leukemic blast cell population is almost completely ineffective, since leukemic blast cells have acquired the characteristic of autonomy, probably due to the several genetic alterations exibited (Seminars in Hematol 32: 201-219, 1995). As demonstrated several years ago, the growth fraction of a leukemic population is extremely low because the large majority of AML blast cells do not proliferate actively. Actually, it was observed that AML blast cells are not quiescent, i.e in the Go state, but are blocked at the G1 phase of the cell cycle and loose the capability to progress through the S phase and, therefore, through the cycle (Cancer Res. 46: 5162-5166, 1986; Leukemia 3: 423-430, 1989). Leukemic blast cells accumulation in G1 determines an unbalance between the pool of cells in the cycle and the cells leaving the cycle to enter terminal differentiation. It is therefore evident that the blast cells proliferation advantage is not caused by an increased proliferative capacity, but mainly to the differentiation block, an increased half-life (approx. 25-35 days) (Eur. J. Clin. Invest., 2: 259, 1972) and to a reduced rate of apoptosis. Therefore, in acute myeloid leukemia, the high number of circulating blasts is consequent on the increased cell viability (NYAS 663: 202-214, 1992). Ferrari et al. (British J. Haematol 59: 21-25, 1985) found that the c-fes protooncogene is expressed at high levels in the terminal stages of granulocytic differentiation, but no function could be attributed to the product of this protooncogene. Ferrari et al (Cell growth Diff. 1: 543-548, 1990) and Manfredini et al. (J.Exp.Med., 178: 381-389, 1993) also found that the inhibition of the c-fes protooncogene expression could be obtained by antisense oligodeoxynucleotides (AS-ODNs) specific for c-fes protooncogene mRNA. However, the use of AS-ODNs specific for mRNA have some inconveniences, in particular a scarce inactivation efficiency. Acute promyelocytic leukemia (APL) blast cells can be induced to differentiation, in vivo and in vitro, with all-trans retinoic acid (ATRA) (New Engl. J. Med., 234: 1385, 1991). At present, ATRA is used in vivo for therapeutic purposes to obtain APL blasts differentiation. However, along with the differentiating effect, some untoward side effects, e.g. leukocytosis (Blood, 76: 260, 1990) and the capillary permeability syndrome (Am. Int. Med., 117: 292, 1992) are observed. This syndrome, characterized by acute pulmonary edema, renal insufficiency, hypotension, was first observed in patients treated with IL-2. Endothelial injury and leukocytes infiltration of the surrounding tissue are observed in the capillary permeability syndrome. Some authors propose the hypothesis that inflammatory cytokines, such as IL-1, IL-6, IL-8 and TNF.alpha. on one hand (Leukemia, 8: 1750, 1994; Exp. Hematol. 23: 117-125, 1995) and integrines on the other hand may play a role in the pathogenesis of the capillary permeability syndrome. In fact, ATRA has been shown to cause APL blasts activation, and the consequent induction of the expression of inflammatory cytokines (Exp. Hematol., 23: 117, 1995). Differentiation therapy has to last some months, during which complications jeopardizing the treatment efficacy often arise. As already mentioned, one of the most serious inconveniences produced by a long-term treatment with ATRA is the onset in approx. 20% of cases of the capillary permeability syndrome (often associated to severe leukocytosis). These side effects of ATRA therapy can lead to the interruption of treatment or even to the patient's death. A further inconvenience often arising during a long-term differentiating treatment with ATRA is the onset of a drug resistance mechanism, whereby the treatment obviously becomes ineffective (Blood 82: 2175-2181, 1993). It is, therefore, extremely important to find new products or develop new therapeutic strategies, capable of avoiding the aforementioned drawbacks, or improve the products already known, for an adjuvant treatment of leukemia.